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Am J Physiol Renal Physiol 274: F573-F579, 1998;
0363-6127/98 $5.00
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Vol. 274, Issue 3, F573-F579, March 1998

Nitroflurbiprofen, a new nonsteroidal anti-inflammatory, ameliorates structural injury in the remnant kidney

Clarice Kazue Fujihara1, Denise Maria Avancini Costa Malheiros1, José Luís Donato2, Anicleto Poli2, Gilberto De Nucci2, and Roberto Zatz1

1 Renal Division, Department of Clinical Medicine, University of São Paulo School of Medicine, 01246-903 São Paulo; and 2 Department of Pharmacology, State University of Campinas School of Medicine, 13081-970 Campinas, Brazil

Cyclooxygenase derivatives and nitric oxide (NO) may influence the pathogenesis of progressive nephropathies. We investigated the effect of nitroflurbiprofen (NOF), a NO-releasing nonsteroidal anti-inflammatory drug (NSAID) without gastrointestinal toxicity, in rats with 5/6 ablation (NX). The following four groups were studied: Sham, sham-operated rats; Sham + NOF, Sham receiving oral NOF two times daily; NX, rats subjected to NX; and NX + NOF, NX receiving NOF. NOF was barely detected in plasma but released the parent compound flurbiprofen. At 30 days, glomerular hydraulic pressure (PGC) was 76 ± 3 mmHg in NX (52 ± 1 in Sham, P < 0.05). NOF slightly reduced PGC to 69 ± 2 mmHg in NX + NOF (P > 0.05 vs. NX). Glomerular volumes behaved similarly. At 60 days, tail cuff pressure was 152 ± 6 mmHg, glomerulosclerosis index was 22.1 ± 9.5, and interstitial fractional area was 9.9 ± 1.2% in NX. NOF reduced these parameters to 137 ± 4 mmHg, 3.5 ± 0.7, and 6.4 ± 0.8%, respectively (P < 0.05), without causing growth stunting or anemia. These beneficial effects could not be ascribed to NO donation and may reflect cyclooxygenase inhibition. This is the first evidence that chronic NSAID treatment may ameliorate progressive nephropathies.

renal ablation; kidney failure; chronic pathophysiology; nonsteroidal anti-inflammatory drugs; cyclooxygenase; glomerulosclerosis


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